We have showed that linoleic acid (n-6 polyunsaturated fatty acid) has promoting effect on azoxymethane-induced colon carcinogenesis by increasing the fecal bile acids, especially that of lithocholic acid which is thought to be a promoter of colon carcinogenesis. On the other hand, EPA (n-3 polyunsaturated fatty acid) has inhibitory effect on colon carcinogenesis by suppressing the excessive production of prostaglandin E_2, which may be accompanied with neoplastic formation. Furthermore, EPA also has inhibitory effect on N-nitroso-N-methylurea-induced mammary carcinogenesis and primary tumor growth and lung metastasis of implanted Lewis lung carcinoma (3LL). Here, to shed light on the underlying mechanism, the effect of EPA on 1) prostaglandin metabolism in mammary tumor, 2) the ornithine decarboxylase (ODC) activity and bile acids metabolism on colon carcinogenesis and 3) prostaglandin metabolism and ^3H-thymidine incorporation in 3LL tumor cells were studied. The results showed that 1) EPA reduced the production of PGF_<2alpha> 6-keto-PGF_<1alpha>, and TXB_2 besides PGE_2 in mammary tumors as was showed in colon carcinogenesis, 2) EPA reduced ODC activity in colon tumor and mucosa as well as total and secondary bile acid output in the feces in colon carcinogenesis, 3) EPA reduced ^3H-thymidine incorporation and production of prostaglandins in implanted 3LL tumor cells when compared with linoleic acid and stearec acid (saturated fatty acid). Above findings suggest that EPA will exert its inhibitory effect by modulating lipid and prostaglandin metabolisms in mammary carcinogenesis and in the growth and metastasis of implanted tumor. Moreover, EPA will reduce the colon carcinogenesis not only by prostaglandin synthesis but changing the bile acids metabolism.